Chicago Childhood Diabetes Registry

描述（由申请人提供）：最近儿童糖尿病的增加提出了一个紧迫的公共卫生挑战：尽快开展有效的一级和二级预防工作。因此，我们必须了解当前流行病的潜在机制，特别是遗传学与行为危险因素流行病学变化的相互作用。我们建议调查受影响的先证者及其家庭成员中儿童糖尿病风险的决定因素。这是基于人口的芝加哥儿童糖尿病登记处的竞争延续申请。该数据库代表了全球最大的非西班牙裔黑人糖尿病儿童数据库，也是美国大陆最大的拉丁裔儿童数据库。正在进行的事件病例的确定将提供基本的流行病学数据，并将在受影响儿童的家庭中进一步努力锚，以描述家族内遗传和疾病易感性等位基因表达方面的青年发病葡萄糖耐受不良谱。我们将具体讨论这些假设： 1.青年糖尿病是由一系列病因过程引起的，从自身免疫性1型胰岛素减少症到肥胖相关的胰岛素抵抗2型糖尿病。一部分儿童表现出混合病因学，由于遗传易感性、肥胖和/或身体活动不足而存在胰岛素抵抗，从而加剧了自身免疫性β细胞破坏。 2.儿童糖尿病流行病学的长期变化与1型和2型危险因素的患病率变化直接相关，包括肥胖、缺乏运动和围产期暴露。 3.在年轻糖尿病患者中，特定性状的家族聚集性影响慢性并发症的风险，超过血糖控制。最终，这种方法将允许一个真正的基于人群的分子流行病学研究早发性糖尿病的家庭从一系列的种族群体。

DESCRIPTION (provided by applicant): Recent increases in childhood diabetes present an urgent public health challenge: to mount effective primary and secondary prevention efforts as soon as possible. We must therefore understand the mechanisms underlying the current epidemic, particularly the interaction of genetics with the changing epidemiology of behavioral risk factors. We propose to investigate the determinants of childhood diabetes risk in affected probands and their family members. This is a competing continuation application for the population-based Chicago Childhood Diabetes Registry. This database represents the largest number of non-Hispanic black children with diabetes worldwide, and the largest patient database for Latino children in the continental US. Ongoing ascertainment of incident cases will provide basic epidemiologic data and will anchor a further effort, in families of affected children, to describe the spectrum of youth-onset glucose intolerance in terms of inheritance and the expression of disease susceptibility alleles within families. We will specifically address these hypotheses: 1. That diabetes in youth is caused by a spectrum of etiologic processes, from the insulinopenia of autoimmune type 1 to obesity-related, insulin-resistant type 2 diabetes. A subset of children demonstrate a mixed etiology, with autoimmune beta-cell destruction aggravated by the presence of insulin resistance due to genetic susceptibility, obesity and/or physical inactivity. 2. That secular changes in the epidemiology of childhood diabetes are directly related to changes in the prevalence of both type 1 and type 2 risk factors, including obesity, physical inactivity, and perinatal exposures. 3. That familial aggregation of specific traits affects the risk of chronic complications in young people with diabetes, over and above that of glycemic control. Ultimately, this approach will permit a truly population-based molecular epidemiologic study of early-onset diabetes in families from a range of ethnic groups.